EVERYONE Will Get Finasteride Side-Effects Eventually

Micky_007

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"funny" things is we know more about Cosmos than endocrinology.

One other critical aspect of it when it comes to hair loss and what men are willing to undergo, is the age at which it happens. In my case, having good hair all through my 20s and then a manageable (yet aware of) hair situation through my 30s, simplified things and gave me the time and opportunity to take step back and think about it. Had it been occuring in my early 20s, I would have probably been more desperate, more risk taking and value hair more than other things. I feel like the world of hair loss is unfairly treating everyone in a cookie cutter sort of way and not taking into account the age at which it occurs. That makes such a huge difference and requires a different way to deal with it.

I believe Kintor Pharmaceuticals will be the first to make significant changes in system. We're already seeing it with the speed at which Pyrilutamide is flying through the clinical trials at unprecedented speeds.

I'm definitely not Chinese but I do respect the way China does certain things. Their very serious work ethic and ability to not be influenced by external standards and corruption is definitely one of a kind and I believe it will be the reason we get better treatment than we currently have first coming out from Kintor.

Pyrilutamide and GT20029 are the ones im really interested in from Kintor Pharmaceuticals. Pyrilutamide is already is soon to be in Phase 3 in China and GT20029 has already started a Phase 1.

If all goes well we should be Pyrilutamide around 2023 or at best around late 2022.

What I find interesting is that they claim to not have the side effects of Propecia as they are using another method to deal with DHT that doesn't prevent DHT production but rather deal with the AR sensitivity to DHT by creating an AR Receptor Antagonist with Pyrilutamide and an AR degrador with GT20029.

Since DHT is important and we've seen inhibiting the production of DHT causes a ripple effect of health problems, I find the alternative solutions by Kintor and Pyrilutamide very interesting.
 
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Micky_007

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I believe the prolactin approach is very interesting and promising. SMI could be a real game changer, let's see how the group trial goes...

I do also find this interesting. Are there no companies actually trying the prolactin approach in the pipeline?
 

Pigeon

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I do also find this interesting. Are there no companies actually trying the prolactin approach in the pipeline?
Yes, check this thread:


And this one:


There's also a discord with a lot of information about prolactin and its effects on hairloss.
 
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Micky_007

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Pigeon

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Can we join the Discord? Would be easier to see relevant information there
I think it's closed now, if they intend to do a new groupsbuy I'm sure they'll open it up again. Really a lot of good information there but you'll find a lot of it in the threads. Very promising imo.
 

blue16

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My guess is that the finasteride is GENERALLY safe for the majority of people, but I'll pass for now. For me, there are way too many unknowns, and possible subtle side effects in taking an oral medication that changes your levels of hormones.

Aside from the obvious ED stuff, I've heard a lot of anecdotal reports of fatigue. I also read a study that showed finasteride users were more likely to experience sleep disturbances compared to placebo. Plus the potential cognitive issues.

And my concern is that although these side effects might not be severe, they could be subtle enough to brush off but actually have a noticeable impact on your day. There are too just too many potential subtle side effects that might have an impact on various aspects on one's life. I'd rather not worry about these issues and go another route.

For those that truly don't have any side effects, or are willing to take the risk of unknown side effects, then I wish them nothing but the best of luck.
 

user394587

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My guess is that the finasteride is GENERALLY safe for the majority of people, but I'll pass for now. For me, there are way too many unknowns, and possible subtle side effects in taking an oral medication that changes your levels of hormones.

Aside from the obvious ED stuff, I've heard a lot of anecdotal reports of fatigue. I also read a study that showed finasteride users were more likely to experience sleep disturbances compared to placebo. Plus the potential cognitive issues.

And my concern is that although these side effects might not be severe, they could be subtle enough to brush off but actually have a noticeable impact on your day. There are too just too many potential subtle side effects that might have an impact on various aspects on one's life. I'd rather not worry about these issues and go another route.

For those that truly don't have any side effects, or are willing to take the risk of unknown side effects, then I wish them nothing but the best of luck.
Just playing devil's advocate here, but a lot of people initially think like you do until their hair loss progresses to a certain point, and then they take it out of desperation.
 

Manochoice

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Just playing devil's advocate here, but a lot of people initially think like you do until their hair loss progresses to a certain point, and then they take it out of desperation.
"A lot of people" is such an ambiguous statement and hard to quantify and it became such a deceiving statement due to being the preferred way of former president to bs. But yes, a lot will and a lot won't. Best is to be informed and to take a well contemplated decision than just a rush of the moment.
 

user394587

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"A lot of people" is such an ambiguous statement and hard to quantify and it became such a deceiving statement due to being the preferred way of former president to bs. But yes, a lot will and a lot won't. Best is to be informed and to take a well contemplated decision than just a rush of the moment.
Well my intent certainly wasn't to be "deceiving", I've just seen a lot-...

I've just seen people do this, and the most common thing I hear from them is "I wish I had taken this when I had more hair to save". Of course, you also get people who say taking it was the worst decision they made, and that it ruined their life, which is why I agree that being informed is the most important aspect about decisions such as this. I think everyone can agree with that.
 

blue16

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Just playing devil's advocate here, but a lot of people initially think like you do until their hair loss progresses to a certain point, and then they take it out of desperation.

Agreed. My hairloss isn't horrible (yet) and Rogaine has been able to sustain it so far. But I could definitely imagine a situation where if it is literally a choice between finasteride or not having hair, I might fall in the same category.
 

Feelsbadman

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That is something you set for yourself and wishes can come true
??
im already ugly and baldin wouldn't suit me at all

ill take my chances with finasteride
your tissue is already grown in adult hood finasteride cant reduce the size of your dick
 

Feelsbadman

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i don't understand how it redues your dik size?
i take supplements and eat a diet full of nitrates, een with finasteride i get throbbing erection and have huge veins in my c***
 

Jeju

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i don't understand how it redues your dik size?
i take supplements and eat a diet full of nitrates, een with finasteride i get throbbing erection and have huge veins in my c***
Are you okay, mate? You posted earlier that you miss having a sex drive but now you’re saying you have a throbbing erection with huge veins.
 

Pigeon

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Another interesting piece about FDA:


"The bar for “safe” is equally low, and over the past 30 years, approved drugs have caused an epidemic of harmful side effects, even when properly prescribed. Every week, about 53,000 excess hospitalizations and about 2400 excess deaths occur in the United States among people taking properly prescribed drugs to be healthier.


Prescription drugs are the 4th leading cause of death.


This evidence indicates why we can no longer trust the FDA to carry out its historic mission to protect the public from harmful and ineffective drugs. Strong public demand that government “do something” about periodic drug disasters has played a central role in developing the FDA.2 Yet close, constant contact by companies with FDA staff and officials has contributed to vague, minimal criteria of what “safe” and “effective” mean."
 

Pigeon

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Found some very interesting studies about the importance of DHT:




DHT is an estrogen (receptor) antagonist​


A neat little study, and in-vivo at that, which demonstrates that DHT is a direct estrogen receptor (ER) antagonist. According to the study, so are testosterone, nandrolone and a few other steroids with demonstrated therapeutic effects on ER-positive breast cancer (BC). However, all of the other steroids mentioned by the study are aromatizable and as such suboptimal as anti-estrogens compared to DHT. This is probably one of the reasons that back in the 1960s when synthetic steroids for treatment of BC were first developed, only DHT derivatives such as Proviron and Masteron eventually made it to clinical trials and got approval for this condition. None of the aromatizable synthetic androgens (or testosterone for that matter) made it through the clinical trials despite being much more widely used (experimentally) for BC at the time. When we also consider the fact that DHT (and other 5-AR derives steroids) are also aromatase inhibitors, it becomes clear that DHT is right up there with progesterone in terms of importance for estrogen antagonism, and perhaps the main anti-estrogen in males. Another interesting finding of the study was that the anti-estrogenic effects of DHT were independent from its role as an androgen agonist. However, androgen agonists are well-known known to have anti-estrogenic effects of their own, so the effectiveness of DHT as an anti-estrogen is actually amplified by its role as a strong androgen. Finally, the study provide some information on what a physiological dose of DHT would be, which is subject to much debate in the literature and in the blogosphere. As the study states, healthy males produce about 45 mcg estrogen daily and DHT amounts need to be about 50 times higher in order to fully block the effects of a given amount of estrogen. This means that a daily physiological dose is about 2mg for healthy adult males, and that dose may need to be increased with increasing age or pathological conditions resulting in elevated estrogens such as liver disease, diabetes, prostate cancer, etc.

https://pubmed.ncbi.nlm.nih.gov/6542571/

“…Estrogen treatment to such mice stimulates breast growth and as in other species increases the amount of progesterone receptor in the breast. Both effects of estradiol can be inhibited by dihydrotestosterone. We concluded that this might be an adequate model system for investigating the mechanism of the antiestrogenic action of androgen, and we designed experiments to assess two mechanisms that have been proposed for this action, namely that androgen acts at the genomic level via its own receptor to block estrogen action or that androgen acts as a pharmacological antagonist and/or weak estrogen agonist by competing with estradiol for the estrogen receptor. The findings in these experiments favor the latter possibility. Indeed, the fact that dihydrotestosterone was equally effective in blocking estrogen effects in tfm/Y and control mice suggests that this action of androgen is not mediated by the androgen receptor. If this interpretation is correct, then this effect of androgen is different than the antiestrogenic effect of the hormone in the embryonic mouse breast (11) and in the uterus (12). Dihydrotestosterone binds weakly to the estrogen receptor in mouse breast and like some other antiestrogens appears to anchor the estrogen-receptor in the nucleus of the cell. These effects have only been studied with pharmacological amounts of hormone, but the fact that the relative binding affinities of dihydrotestosterone, 313-androstanediol, testosterone, and Sfdihydrotestosterone correlate with their capacities to inhibit induction of the progesterone receptor is in keeping with the finding in MCF7 tumor cells (10) that androgens bind to the estrogen receptor. Unlike the situation in MCF7 cells, however, we were unable to demonstrate any estrogen-like effects of dihydrotestosterone on the mouse breast.”
“…If androgen prevents the development of gynecomastia in normal men by acting as a direct antiestrogen at the level of the estrogen receptor, this is the first androgen action recognized that is not mediated by the androgen receptor.”
“…Normal men produce ~45 mcg of estradiol each day, a sixth of which is secreted by the testes and the remainder of which is derived from the extraglandular aromatization of circulating androgens (1). Extraglandular estradiol formation takes place by two mechanisms, one from the direct conversion of testosterone to estradiol and the other from androgens of adrenal origin by the sequence of androstenedione – estrone – estradiol. The function of estradiol in normal men is unknown, but feminization, commonly manifested by gynecomastia, ensues under conditions of relative or absolute estrogen excess (2)….By this estimate estradiol binds to the estrogen receptor with an affinity that is approximately fifty times greater than that of dihydrotestosterone.”







Low DHT can cause hypogonadism symptoms even in eugonadal men​


Seemingly contradictory title, but the study findings are pretty clear. Namely, even in males with normal testosterone levels there is a direct inverse relationship between DHT levels and symptoms of hypogonadism such as sexual dysfunction and “aging male” syndrome. For every 10% increase in DHT levels there was a 4.67% decrease in hypogonadism symptoms of eugonadal males. So, once again, this is evidence that testosterone (T) is little more than a pro-hormone produced in the gonads and peripheral tissues and that its metabolite DHT is the primary androgen responsible for health of males.

https://pubmed.ncbi.nlm.nih.gov/33811609/

“…Results: Serum total/free T as well as dihydro-T (DHT) was associated with IIEF-EF and AMS scores in the overall population using univariate analyses. Multivariate approaches revealed DHT concentrations in subjects with normal T levels (n = 416, Total T > 12 nmol/L) to be significant predictors of AMS scores. A 0.1 nmol/l serum DHT increase within the eugonadal range was associated with a 4.67% decrease in odds of having worse symptoms (p = 0.011). In men with biochemical hypogonadism (Total T < 12 nmol/L), total and free T rather than DHT were associated with AMS results. This association was not found for IIEF-EF scores. Indirect effects of age and BMI were seen for relations with hormone concentrations but not questionnaire scores. Conclusion: DHT can be associated with symptoms of hypogonadism in biochemically eugonadal men. Serum DHT measurement might be helpful once the diagnosis of hypogonadism has been ruled out but should not be routinely included in the primary diagnostic process.”
 
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